micro chapter 17, unit 4

hypersensitivities

Immune responses that cause tissue injury

Autoimmune disease

occurs when the immune system attacks self-antigens

1. —Type I: Immediate IgE-mediated

2. —Type II: Cytotoxic

3. —Type III: Immune Complex-mediated

4. —Type IV: Delayed Cell-mediated

what are the 4 major times of hypersensitivities

Type I hypersensitivity

characterized by an allergic reaction in a sensitized individual within minutes of exposure to an antigen

ex anaphylactic shock, hay fever, hives, and asthma

Mechanism of Type I Hypersensitivity

• —A person becomes sensitized with first exposure to antigen (allergen).

• —B cells that are committed to producing IgE are activated by the antigen.

• —IgE activates mast cells or basophils upon second exposure to the antigen.

• —Mast cells and basophils release histamine and other cytokines.

• Symptoms are related to the activity of histamine

Desensitization

Desensitization is a process where a patient is given gradually increasing doses of an allergen, starting at very low levels. This stimulates production of IgG antibodies, which bind the allergen before IgE, preventing mast cell activation and reducing the risk of anaphylaxis.

Type II hypersensitivity reactions

antibodies trigger the destruction of human cells

ex transfusion reactions and hemolytic disease of the newborn (erythroblastosis fetalis)

—Transfusion Reactions

When an individual receives a transfusion of RBC’s that are antigenically different from his/her own (A, B, O, etc) the immune system destroys those cells

—Hemolytic Disease of the Newborn

IgG antibodies against Rh antigen are produced by an Rh- mother following delivery of her first Rh+ child.

During subsequent pregnancies with Rh+ children, IgG antibodies cross the placenta and destroy fetal RBC’s

what is type III hypersensitivity and how can it cause disease

An immune complex is formed when IgG or IgM antibodies bind to antigens. Normally, they are cleared by macrophages, but when produced in excess, they deposit in small blood vessel walls (basement membranes), activate complement, and cause inflammation and tissue damage.

Examples of Type III hypersensitivity

post-streptococcal glomerulonephritis, Arthus reaction, and serum sickness

Type IV hypersensitivity is a T cell–mediated (delayed) immune response where sensitized T cells release cytokines, recruiting macrophages and causing inflammation. This leads to rash, blistering, and scaling in contact dermatitis. Common allergens include poison ivy/oak, metals, cosmetics, and latex.

What is Type IV hypersensitivity and how does it cause contact dermatitis?

Type IV Hypersensitivity

—Delayed hypersensitivity results from the harmful effects produced by cell-mediated immunity.

The reaction peaks at 2-3 days rather than in minutes (as with Type I).

ex contact dermatitis, granuloma formation, and graft rejection

tuberculosis, leprosy, and histoplasmosis

what are the 3 infections that are responsible for granulomas?

granuloma

walls off intracellular infectious organisms, preventing the infectious microbe from escaping to infect other cells

Autoimmune disease

when the immune system responds to tissues of the body as if they were foreign

Immunodeficiency

when the body is incapable of making or sustaining an adequate immune response

2 categories

• Primary Immunodeficiency

• Secondary Immunodeficiency

Primary Immunodeficiency

genetic or developmental abnormalities result in dysfunctional B or T lymphocytes.

Secondary Immunodeficiency

result from environmental, rather than genetic, factors.

Caused by malignancies, advanced age, viral infections, immunosuppressive drugs, or malnutrition

DiGeorge syndrome (Primary Immunodeficiency)

the thymus fails to develop.

Therefore, T cells do not mature. Individuals suffer from repeated infections with eukaryotic pathogens, viruses, and obligate intracellular bacteria

Severe combined immunodeficiency(SCID) (Primary Immunodeficiency)

neither T nor B lymphocytes are produced in the bone marrow.

Children with SCID die of infectious disease at an early age without bone marrow transplant.